Altered expression of CD4, CD54, CD62L, and CCR5 in primary lymphocytes productively infected with the human immunodeficiency virus

Infection of T cells with HIV-1 induces loss of CD4 and HLA class I from th e cell surface. In the present article we have investigated whether changes in expression of other cell surface molecules could be related to HIV infe ction. To detect HIV-infected cells at the single-cell level, peripheral bl ood lymphocytes were infected in vitro with HIV-HSA, a reporter virus encod ing the murine heat-stable antigen. Expression of HSA on activated primary lymphocytes was an efficient indicator of productive infection. Expression of the majority of the cell surface proteins studied was unaffected by HIV infection (HLA class I, II, CD11a, CD18, CD25, CD27, CD28, CD29, CD30, CD31 , CD38, CD44, CD45R0, CD49d, CD57, CD94, CD95, and CXCR4). However, phenoty pic changes specific to the productively infected cells were detected. Expr ession of the CD4 molecule was progressively lost and this was closely asso ciated with loss of CD62L expression, a molecule involved in T cell homing into the lymph nodes. By contrast, T cells productively infected with this T-tropic reporter virus were enriched for CD54, and for CCR5, the main core ceptor for M-tropic viruses. Given the roles of CD62L, CD54, and CCR5 in ly mphocyte trafficking, these results suggest that cells productively infecte d with HIV might have altered homing patterns in vivo.